Document Detail

Regulation of HOXA-10 expression by testosterone in vitro and in the endometrium of patients with polycystic ovary syndrome.
MedLine Citation:
PMID:  12519859     Owner:  NLM     Status:  MEDLINE    
Polycystic ovary syndrome (PCOS) affects approximately 5% of reproductive-age women and is characterized by anovulation and increased androgen production. Despite the ability to correct ovulatory disorders, pregnancy rates remain paradoxically low, and spontaneous pregnancy loss rates are high. To determine whether uterine dysfunction contributed to the adverse reproductive outcomes in PCOS, we assessed the effect of the increased ovarian androgens on a well-characterized gene essential to endometrial receptivity. Up-regulation of HOXA10 in the endometrium is necessary for receptivity to embryo implantation. In vitro, HOXA10 expression was repressed by testosterone but not by dehydroepiandrosterone, dehydroepiandrosterone sulfate, or insulin. Testosterone also prevented the increased expression of HOXA10 previously reported with estradiol or progesterone. Dihydrotestosterone produced an effect similar to that of testosterone, whereas flutamide blocked the testosterone effect. Endometrial biopsies, obtained from women with PCOS, demonstrated decreased HOXA10 mRNA. Testosterone is a novel regulator of HOXA10. Diminished uterine HOXA10 expression may contribute to the diminished reproduction potential of women with PCOS.
Dilek Cermik; Belgin Selam; Hugh S Taylor
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  88     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-01-09     Completed Date:  2003-02-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  238-43     Citation Subset:  AIM; IM    
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
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MeSH Terms
Cell Line
Endometrium / drug effects*,  metabolism*
Homeodomain Proteins / genetics,  metabolism*
Polycystic Ovary Syndrome / metabolism*
RNA, Messenger / metabolism
Testosterone / pharmacology*
Grant Support
Reg. No./Substance:
0/Homeodomain Proteins; 0/RNA, Messenger; 164384-16-1/Hoxa10 protein, mouse; 58-22-0/Testosterone

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